A human ear comprises an outer ear, a middle ear, and an inner ear. The outer ear picks up acoustic pressure waves, which are converted into mechanical vibrations in the middle ear. In the inner ear, a cochlea, which is a snail-shaped cavity filled with cochlear fluid, converts the mechanical vibrations into pressure waves, causing a basilar membrane to displace. This in turn displaces hair cells in contact with the basilar membrane, causing associated biological neurons to fire. These biological neurons communicate with the central nervous system via the auditory nerve to transmit information about the acoustic signal to the brain. The brain then registers the information as perceptions of sound.
Hearing loss, which may be due to many different causes, generally comprises two types: conductive and sensorineural. Conductive hearing loss occurs when the normal mechanical pathways for sound to reach the hair cells in the cochlea are impeded. Conductive hearing loss often may be helped by use of conventional hearing aids, which amplify sound so that acoustic information reaches the cochlea and the hair cells. Sensorineural hearing loss, on the other hand, is usually due to the absence or impairment of the hair cells which are needed to transduce acoustic signals in the cochlea into nerve impulses that are sent to the auditory nerve. People suffering from sensorineural hearing loss are usually unable to derive any benefit from conventional hearing aid systems because their mechanisms for transducing sound energy into auditory nerve impulses are non-existent or have been severely damaged.
Cochlear implant technology seeks to overcome sensorineural hearing loss by bypassing the hair cells in the cochlea and presenting electrical stimulation to the biological neurons directly, leading to the perception of sound in the brain and at least partial restoration of hearing. Cochlear implant technology may be used to bypass the outer, middle and inner ears. Cochlear implant systems that utilize such technology have been successfully used to restore hearing in sensorineurally deaf patients.
Generally, a cochlear implant system includes a power source, a microphone, a signal processing device, a stimulation device and an electrode array, one or more of which may be implanted within the patient. The power source supplies power to the system. Sound enters the system through the microphone which delivers it to the signal processing device as an electrical signal. The signal processing device processes the signal and stimulates electrodes in an electrode array that is implanted in the cochlea based on the processed signals. The electrodes in the array transmit electrical stimuli to the nerve cells or biological neurons associated with the cochlea. These nerve cells are arranged in an orderly tonotopic sequence, from high frequencies near the initial (basal) end of the cochlear coil to progressively lower frequencies towards the inner end of the coil (apex). Nerve cells emanating from the various regions of the cochlea are associated with the frequencies that most efficiently stimulate those regions. The brain, which receives neural impulses from the auditory nerve, maps those frequencies in accord with this association.
Conventional cochlear implants separate sound signals into a number of parallel channels of information, each representing the intensity of a narrow band of frequencies within the acoustic spectrum. Ideally, each channel of information would be conveyed selectively to the subset of nerve cells located along the cochlea that would have normally transmitted information about that frequency band to the brain. The electrode array is typically inserted into the scala tympani, one of the three parallel ducts that make up the spiral shape of the cochlea. The array of linearly arranged electrodes is inserted such that the electrode closest to the basal end of the coil is associated with the highest frequency band and the electrode closest to the apex is associated with the lowest frequency band. Each location along the implanted length of the cochlea may be mapped to a corresponding frequency, thereby yielding a frequency-to-location table for the electrode array. The foregoing illustrates the relationship between frequency and physical location in the cochlea—i.e., the cochlear frequency/location correspondence.
Many pulsatile neural stimulators, particularly in the case of cochlear implant stimulators, employ a fixed-rate stimulation strategy, in which amplitude-modulated current pulses are generated for each channel at a fixed frequency and used to stimulate the implanted electrodes. However, studies have shown that fixed-rate stimulation may differ from biological acoustic stimulation for many reasons. First, biological acoustic stimulation of the cochlea produces much less across-fiber synchrony and much more within-fiber jitter than electrical stimulation from a cochlear implant that employs a fixed rate stimulation strategy. Second, in fixed-rate stimulation, low rate stimulation (less than approximately 800 Hz) causes entrainment of the response—that is, a deterministic neural discharge once per stimulus cycle at the fixed rate of the carrier—and temporally-precise phase-locking to the carrier (i.e., a fixed-rate pulse train), even though the carrier contains no useful information about the sound environment. Those effects do not occur in biological acoustic stimulation. Third, in fixed-rate stimulation, high rate stimulation (greater than approximately 800 Hz) causes neural spiking to occur at highly regular intervals determined by the relative refractory period (that is, the time for a neuron to recover from a previous discharge) and may cause sever distortions in the temporal discharge patterns as a result of neural refractoriness. Studies have shown that the distributions of interspike interval (ISI) and modal period (MP) histograms of fixed rate stimulation systems are concentrated at the refractory period and phase (respectively). Such regular neural spiking and phase are unnatural compared to biological acoustic stimulation, which tend to have ISI and MP histograms that exhibit wider distributions. These effects that are observed in fixed rate stimulation systems stem from neuronal synchronization to the fixed rate of the stimulation carrier and interaction between electrodes.
In view of the foregoing, it would be desirable to be able to provide systems and methods for providing neural stimulation with an asynchronous character. As used herein, the term “asynchronous stimulation” means that the rate or rates at which nerve cells are stimulated are not limited to fixed rate or rates. Thus, the stimulation rate or rates may be adjusted dynamically.
It also would be desirable to be able to provide systems and methods for providing neural stimulation in which each channel is stimulated in a stochastic manner.
It further would be desirable to be able to provide systems and methods for conveying phase information during neural stimulation.
It even further would be desirable to be able to provide systems and methods for providing neural stimulation with reduced power.
It additionally would be desirable to be able to provide systems and methods for providing neural stimulation that more closely resembles biological acoustic stimulation.